Prostate cancer tissue (low-grade by Gleason score) stained with an antibody for a methylated amino acid within histone H4
Photo by David Seligson, courtesy of Siavash Kurdistani, UCLA Department of Biological Chemistry, LA, USA
Cancer affects everyone: young or old, rich or poor. Well over a tenth of global deaths in the year 2000 were caused by malignant tumours. Even if you never get cancer, no doubt you know someone who has or will. A couple of years ago the World Health Organisation estimated that by 2020 cancer rates will have doubled affecting 15 million people worldwide.
Brona McVittie reports :: June 2006
So what of a cure?
The hunt for a 'cure' is complicated by the fact that cancer is not one disease, but an umbrella term for a highly varied collection of disorders. There are over a hundred different kinds – lung cancer being the most common. But even narrowing it down to a specific cancer, the variety in cause and pathology of these conditions is mind-boggling. Needless to say a global cure for cancer remains a distant goal.
On the plus side, we're now much better educated about cancers and their potential causes. Many of us have made lifestyle changes as a result, because we now realise that cure is not the answer. Health services now run screening programmes for breast, cervical and bowel cancer. As a result patients are now presenting much earlier during the disease process, and are much more likely to benefit from treatment.
However, available treatments could do with some improvement. For example, take prostate cancer. There is huge variability between sufferers, and not yet any hard and fast means of assessing what kind of treatment a patient should have. If a man has a low-grade cancer, as measured by the Gleason scoring system, he could still get an aggressive tumour later in life. Should doctors be relying on the Gleason score to decide the extent and duration of chemo? Preferably not, but current options are limited. Luckily epigenetics has recently come up trumps in respect to cancer diagnostics. The enzymes that modify histones behave differently as prostate tumours progress. Scientists can get a good impression by looking at the way histone tails have been tweaked in tumours from different patients. Apparently patterns of global histone modification can serve as an indicator of the future course of disease. Such epigenetic profiling of cancers, coupled with our knowledge of risky mutations, should pave the way for personalising cancer treatments across the board.